Fig. 19.7 can be produced by electrical stimulation of the cardiac sympathetic nerves. When the effects of such neural stimulation are restricted to the heart, the vascular function curve is unaffected. Therefore, only one vascular function curve is needed for this hypothetical intervention (see
Fig. 19.7
During the control state of the model, the equilibrium values for cardiac output and Pv are designated by point A in
Fig. 19.7 . Cardiac sympathetic nerve stimulation abruptly raises cardiac output to point B because of the enhanced myocardial contractility. However, this high cardiac output causes an increase in the net transfer of blood from the veins to the arteries of the circuit, and as a consequence, Pv subsequently begins to fall (to point C). The reduction in Pv then leads to a small decrease in cardiac output. However, cardiac output is still sufficiently high to effect •Fig. 19.8 Duringelectricalstimulationofthecardiacsympatheticnervefibers,aorticbloodflow(cardiacoutput)increased,whereaspressuresintheleftatrium(PLA)andrightatrium(PRA)diminished.Thesedataconformtotheconclusionsderivedfrom
Fig.19.7 ,inwhichtheequilibriumvaluesofcardiacoutputandvenouspressureareobservedtoshiftfrompointAtopointD(i.e.,cardiacoutputincreased,butcentralvenouspressuredecreased)duringcardiacsympatheticnervestimulation.(RedrawnfromSarnoffSJ,etal.Circ Res. 1960;8:1108.) the net transfer of blood from the veins to the arteries of the circuit. Thus both Pv and cardiac output continue to fall gradually until a new equilibrium point (point D) is reached. This equilibrium point is located at the intersection of the vascular function curve and the new cardiac function curve. In
Fig. 19.7 , point D lies above and to the left of the control equilibrium point (point A) and indicates that sympathetic stimulation can evoke greater cardiac output despite the lower level of Pv.
The biological response to enhancement of myocardial contractility is mimicked by the hypothetical change predicted by the model in this chapter. As depicted in
Fig. 19.8 , sympathetic nerves innervating the heart are stimulated during the time denoted by the double-headed arrow. During neural stimulation, cardiac output (aortic flow) rises quickly to a peak value and then falls gradually to a steady-state value significantly higher than the control level. The increase in aortic flow is accompanied by reductions in right and left atrial pressures.
Changes in blood volume do not directly affect myocardial contractility, but they do influence the vascular function curve in the manner shown in
Fig. 19.4 . Thus to understand how changes in blood volume affect cardiac output and Pv, the appropriate cardiac function curve is plotted along with the vascular function curves that represent the control and experimental states (
Fig. 19.9 ). When blood volume is increased by a blood transfusion, the equilibrium point (point B in
Fig. 19.9 ), which denotes the values of cardiac output and Pv after transfusion, lies above and to the right of the control equilibrium point (point A). Thus transfusion increases both cardiac output and Pv. Hemorrhage causes the opposite effect. Mechanistically, the change in ventricular filling pressure (Pv) evoked by a given change in blood volume alters cardiac output by changing the sensitivity of the contractile proteins to the prevailing concentration of intracellular Ca++ (see ). For reasons explained earlier, pure increases or decreases in venomotor tone elicit responses that are like those evoked by increases or decreases, respectively, in total blood volume.
•Fig. 19.9 Afterabloodtransfusion,thevascularfunctioncurveisshiftedtotheright.Therefore,bothcardiacoutputandvenouspressureareincreased,asdenotedbytranslocationoftheequilibriumpointfrompointAtopointB.–2 A B 1086420 0 2 4 6 8 10 Central venous pressure (mm Hg) Transfusion ControlCardiac output (L/min)